Role of Agmatine in Mitochondrial Homeostasis: implication for Neurodegenerative disorders

Abstract

Mitochondrial dysfunction is a hallmark feature of various neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease, contributing to disease progression and neuronal degeneration. Agmatine, a naturally occurring polyamine, has garnered attention for its potential role in maintaining mitochondrial homeostasis and its implications for neurodegenerative disorders. This review provides a comprehensive overview of the current understanding of agmatine's biochemical properties, physiological functions, and its mechanisms in regulating mitochondrial homeostasis. We discuss evidence supporting the therapeutic potential of agmatine in mitigating mitochondrial dysfunction, including its effects on mitochondrial biogenesis, dynamics, oxidative stress, and apoptosis pathways. Furthermore, we highlight experimental studies and clinical trials investigating the efficacy of agmatine in cellular and animal models, as well as its translation into clinical applications for neurodegenerative disorders. Despite promising preclinical findings, challenges and limitations in clinical translation are also discussed. Finally, we propose future research directions and emphasize the significance of agmatine as a promising therapeutic strategy for targeting mitochondrial dysfunction in neurodegenerative disorders.